Guillain-Barre syndrome (GBS) is an acute, immune-mediated, motor-sensory polyneuropathy (AIP) that typically has evidence of demyelination on electrodiagnostic or pathological studies (Asbury, A. K., and McKhann, G. M., Ann. Neurol 41:287-288 (1997); Asbury, A. K., and Comblath, D. R., Ann. Neurol. 27suppl:S21-4 (1990)). Other AIP syndromes have selective motor (McKhann, G. M. et al., Ann. Neurol. 33:333-342 (1993)), cranial nerve (Fisher, M., N. Engl. J. Med. 255:57-65 (1956)), or axonal involvement (Feasby, T. E. et al., Brain 109:1115-1126 (1986)). In acute motor axonal neuropathy (AMAN) (Kornberg, A. J. and Pestronk, A., Muscle Nerve 17:100-104 (1994)) and Miller-Fisher syndrome (Chiba, A. et al., Ann. Neurol. 31:677-679 (1992)), antibodies directed against neural antigens, such as glycolipids, have been reported in 30% to 90% of patients; however, serum antibodies, with some disease specificity and directed against purified neural antigens, have not been consistently identified in most motor-sensory GBS syndromes with demyelinating features (Hartung, H. P. et al., Muscle Nerve 18:137-153 (1995); Rostami, A. M., Spring. Semin. Immunopathol. 17:29-42 (1995); Vriesendorp, F. J. et al., Ann. Nerol. 34:130-135 (1993); Ilyas, A. A. et al., Ann. Neurol. 23:440-447 (1988); Willison, H. J. and Kennedy, P. G., J. Neuroimmunol. 46:105-112 (1993)).
Because polyneuropathies are potentially treatable, correct identification of a patient's particular polyneuropathies is important. Methods of diagnosing such polyneuropathies based on specific disease-related criteria would facilitate identification of treatable disease and expedite commencement of treatment.